Post-Operative Chapters 21 and 22

Dr. Vasanthi Vidyasagaran*

Department of Anaesthesiology, Kauvery Hospital, Chennai, Tamilnadu, India

POST-OPERATIVE Chapter 21

Respiratory Obstruction Due to Adenoid Pack

An eight-year-old boy, weighing 30 kilograms was posted for Adeno-tonsillectomy. On examination, his lungs were clear, airway showed Mallampati Class 2, and pulse rate of 108 beats/min. All his investigations were within normal limits. He was taken up for surgery under general anaesthesia. He was pre-medicated with injection Glycopyrrolate 0.1 mg, half an hour before surgery. Aspiration prophylaxis (Ranitidine 25 mg + Ondansetron 2mg) was given.

He was pre-oxygenated for 3 minutes and induced with Thiopentone 150 mg and Fentanyl 50 µg. For intubation, 20 mg Atracurium was used. Sevoflurane 2%, Oxygen and Nitrous Oxide mixture was used for maintenance. Standard monitoring was done.

The surgery lasted 35 to 40 minutes and no more relaxants were given. At the end of procedure, he was reversed with Neostigmine 1 mg and Glycopyrrolate 0.1 mg. After ensuring adequate breathing, he was extubated in a deep plane. There was no post nasal bleeding and the gauze count was mentioned to be correct.

Post extubation, patient started to desaturate. Respiration was noisy and there was in-drawing of the ribs. Laryngospasm was suspected and intravenous hydrocortisone 50 mgs was given. CPAP was attempted, but did not relieve the obstruction. Saturation dropped to 90%. It was impossible to mask ventilate and there was unexpected tightness of the bag. The child was still quite well sedated. He was re-intubated using 50 mg Suxamethonium. The bag compliance improved and saturation went up to 100%. Nasal endoscopy did not reveal anything abnormal.

The boy began to come out of the effect of Suxamethonium, and at this point laryngoscopy revealed a blood soaked adenoid pack coming into the oral cavity which was removed. The reason for upper airway obstruction came into light. The child recovered well without further complications.

Discussion

Here was a situation of upper airway obstruction due to adenoid gauze pack left behind at the end of surgery. A wrong gauze count misled the team. Although the anaesthesiologist had checked all parameters prior to extubation in deep plane, this was not visible during laryngoscopy at extubation.

Such incidents happen even during third molar tooth extractions, where the throat pack is removed, but the gauze is often left behind.

Laryngospasm may be the most common cause of post extubation problems, but other causes including iatrogenic, must be ruled out, without any delay.

Points to Ponder

Is extubation under deep plane of anaesthesia, worth it and safe? Particularly in a child, this can be very tricky.

How deep a plane is safe for extubation? This may be learnt as a special skill over years of experience, however it remains controversial. Extubation when the patient is deep risks aspiration and loss of airway control. Light plane may risk spasm.

Extubation in the deep plane can be considered in surgeries not involving the airway. In this particular incident, the child could have easily aspirated the soaked gauze. It is important not to blindly trust the count especially if it is involving the airway. It is vital for the anaesthetist to check for themselves by direct laryngoscopy.

Extubation following laryngoscopy is the preferred method in all head and neck surgeries. The key principle in the management of all post-extubation airway problems is immediate and effective oxygenation.

Awake extubation is always the safe method of tracheal extubation, especially in a child having upper airway surgery, and I would recommend it. However, more experienced paediatric anaesthetists may prefer to extubate in deep planes.

The debate regarding deep versus awake extubation in paediatrics continues.

Stridor and Stertor: Differentiation is important to identify the level of obstruction.

Stridor is an abnormal, high-pitched sound produced by turbulent airflow through a partially obstructed airway at the level of the supraglottis, glottis, subglottis, or trachea. Inspiratory stridor suggests a laryngeal obstruction, expiratory stridor implies tracheobronchial obstruction and a biphasic stridor suggests a subglottic or glottis anomaly.

Stertor, on the other hand is a lower-pitched, snoring-type sound generated at the level of the nasopharynx, oropharynx, and, occasionally, supraglottis.

References

Swati Karmarkar, Seema Varshney; Tracheal extubation. Continuing Education in Anaesthesia, Critical Care & Pain | Volume 8 Number 6 2008
Peterson GN, et al., Management of the difficult airway: a closed claims analysis. Anesthesiology2005; 103:33-9.
Baijal RG, Bidani SA, Minard CG, Watcha MF. Perioperative respiratory complications following awake and deep extubation in children undergoing adenotonsillectomy. Paediatr Anaesth. 2015 Apr; 25(4):392-9.
Popat M, Mitchell V, Dravid R, Patel A, Swampillai C, Higgs A. Difcult Airway Society Guidelines for the management of tracheal extubation. Anaesthesia 2012; 67: 318–340

POST-OPERATIVE Chapter 22

Sickle Cell Anaemia – A Surprise in the Immediate Post-operative Period

A 30-year-old primiparous woman, weighing 74 kg was diagnosed with pre-eclampsia. She was on treatment with tablet Labetalol 20 mg twice daily and was posted for an elective caesarean section at 38 weeks gestation.

During preoperative evaluation, she was found to have sickle cell disease. Her Hb was 10 gm%, PCV=31%, platelets=1.5 lakh/cu mm, renal, liver functions and coagulation profile were normal.

Following an unanticipated episode of convulsions at home, she had to be taken up for an emergency caesarean section. She recovered from convulsions without any medications. She was brought to the hospital with severe head ache. On admission, she was conscious, her BP was 180/120 mm Hg, PR=110 – regular, respiratory rate=20 breaths/minute. She had bilateral pedal oedema.

She was taken up for an emergency LSCS. As there was no time for further investigations and there was foetal distress, a bedside bleeding and clotting time was performed and found to be normal. Blood grouping and cross matching was done and adequate blood products were made available.

The main concern was whether to choose general or regional anaesthesia. She was a patient with a full stomach, (had solids just before coming to the hospital) airway assessment was anticipated difficult airway with MPC III and protruding maxilla, with limited mouth opening. Spine was normal. Spinal anaesthesia deemed appropriate for this patient. One dose of nifedipine 10mg was given with a sip of water. 1.8 ml of 0.5% Bupivacaine was administered using a 26G needle in the L3-L4 space. The level of block was T6. Usual monitoring was performed and supplemental oxygen was administered via face mask. The surgery was performed uneventfully. Patient was shifted to the post-operative ward.

10 hours later, there was a sudden fall in blood pressure, the patient was getting very anxious and hyperventilating. BP was 80/40. Patient was suspected to have an intra-abdominal haemorrhage and PPH. She was shifted to OT for an emergency laparotomy.

General anaesthesia using Ketamine 50 mg, Fentanyl 100 mcg, and Succinylcholine was administered. Patient was intubated with difficulty using a size 6.5 cuffed oral ETT. Anaesthesia maintained with Oxygen/Nitrous Oxide and 1% Sevoflurane. On opening the abdomen, there was a haemo-peritoneum of 2 litres, but the cause of haemoperitonium was not PPH, but a ruptured spleen! Splenectomy was done without any delay. After initial load of 1 litre of crystalloid, blood transfusion was commenced. She received 6 units packed cells, 4 units FFP and 2 units of platelets without any delay, since she was a case of sickle cell anaemia and the blood products were made available for the caesarean section. Haemodynamics were maintained with inotropic support in addition to volume support.

Early and timely transfusion of blood and blood products as an adjunct to appropriate anaesthetic and surgical management helped stabilise this patient. She was then shifted to PACU on ventilator and inotropic support. She was extubated after 48 hours when she was off inotropes, adequate respiratory function and renal function ensured. Broad spectrum antibiotic cover was provided to prevent sepsis.

Discussion

Sickle cell disease (SCD) is uncommon in the female patient as it is an autosomal recessive disease. Patients with SCD are known to have episodes of crisis triggered by dehydration, pain, and cold temperatures. They should preferably be taken up for elective procedures after investigations and adequate optimisation.

The incidence of PIH is high in sickle cell disease, and low dose aspirin is usually prescribed. Low molecular weight Heparin is advised both pre-and postoperatively to prevent thrombotic complications like acute stroke. Plan of anaesthesia should take into consideration the coagulation status, hydration, anaemia, temperature, and post-operative pain relief, thus avoiding a crisis. Routine prophylactic transfusions are not recommended.

Avoid NSAIDs for pain relief. Among narcotics, Pethidine should be avoided since the metabolite Norpethidine can accumulate and cause seizures.

Splenomegaly in SCD – Splenic enlargement in SCD patients usually occurs in the first decade of life. Later on, they undergo auto splenectomy due to recurrent splenic infarcts and decline in splenic function. However, this is not always the case, enlarged spleen may be noted in older patients with SCD. Immune function will be reduced with reduced splenic function.

Life threatening features of SCD that an anaesthetist may have to face are pain crises, severe sepsis, severe anaemia, acute chest syndrome including pulmonary embolism, splenic sequestration, liver congestion, and aseptic bone necrosis and infarcts.

The question of splenectomy arises when there is strong evidence of life-threatening episodes of acute splenic sequestration, (which cannot be predicted), or sustained hypersplenism which may result in severe anaemia.

It is postulated that factors such as stress, surgery, and pain may act as trigger factors and cause rapid sequestration of blood in spleen, and the vasculature gets obstructed. This causes rapid splenomegaly, requiring emergency intervention as the patient will be in a state of shock. Rapid transfusion of blood and blood products is the only treatment that can save the patient. This is usually a self-resolving crisis, and responds to supportive management and blood transfusion.

However, if there has been a splenic rupture as seen in this patient splenectomy must be done without any delay, taking all precautions to prevent sepsis following splenectomy.

References

Valentine Brousse, Pierre Buffet and David Rees. British Journal of Haematology. The spleen and sickle cell disease: the sick (led) spleen. 2014
Airede, A.I. (1992) acute splenic sequestration in a five-week-old infant with sickle cell disease. Journal of Pediatrics, 120, 160.
Sarika Subhash Ingle and Pravin Ubale. Anesthetic management of a patient with sickle cell disease for common bile duct exploration, J Anaesthesiol Clin Pharmacol. 2011 Oct- Dec; 27(4): 547–549.
Rajab KE, Skerman JH. Sickle cell disease in pregnancy. Obstetric and anesthetic management perspectives. Saudi Med J. 2004 Mar; 25(3):265-76.
Indu Bala, Neeru Sahni, and Sanwar Mal Mitharwal. Anaesthetic challenges in a child with sickle-cell disease and congenital heart block. Indian J Anaesth. 2016 Apr; 60(4): 294–295.
Sickle Cell Disease – Kids Health, kidshealth.org/en/teens/sickle-cell-anemia.html.

Post-Operative Chapters 21 and 22